Cell, in a paper published by researchers from the Max-Planck Institute of Evolutionary Anthropology. In order to advance our understanding of FOXP2, the scientists chose to examine its expression in mice, a surprisingly strong model for many human biological systems. The chief difference in FOXP2 between humans and many other species such as mice boils down to two changes in the gene. At some point in human prehistory, these changes arose and quickly became universal in the FOXP2 of humans. To see what effect those changes might have had, the Max Planck scientists altered the copies of FOXP2 in mice to be identical to the copies of FOXP2 in humans. They then examined any changes that took place surrounding the cognition and vocal skills of the genetically altered mice, to see how they might be affected by the supposedly advanced copy of FOXP2. And, while the linguistic skills of the mice failed to rival our own, the scientists did see some surprising changes. First, they found that the altered mice showed changes in their brain circuitry that bore some similarity to that of humans. And perhaps most intriguing, the altered mice had distinct ultrasonic vocalizations that differed from their unmodified brethren. Ultrasonic vocalizations, sometimes referred to as chirps or squeaks, are used by mice to communicate to each other, such as to warn of a predator. When the young altered mice were separated from their mothers, something that usually elicits many such squeaks, they emitted ultrasonic vocalizations that were distinctly different in intensity and frequency than their counterparts. The authors argue that the altered FOXP2 in the mice was influencing the type of squeaks that they were making when separated from their mothers. And the scientists therefore believe there is some kind of connection to language development. But what does all this mean to humans? The past several years of research into FOXP2 has revealed that human patients who carry at least one non-functional version of the gene (i.e., the version of the gene found in species other than humans) have problems producing the facial movements necessary to form words. It had been thought that part of the function of FOXP2 in humans was to develop motor control needed to articulate our mouths, vocal chords, and esophagus to produce complex language. Many experts have also proposed that FOXP2 in humans plays a role in the development of both the lungs and the esophagus – both of which are vital to speech. This most recent study shows that by simply tweaking FOXP2 in mice, we see a noticeable change in how they communicate. Clearly, there is much more work to be done and many more questions to be answered. In the future, these researchers envision going even further to understand exactly how FOXP2 influences our ability to communicate with each other. Their next goal? To understand the exact mechanics behind the version of FOXP2 found in humans, so that they can finally piece together its importance in giving us the power of speech.